REASONING GP · Clinical algorithm · Quick reference

Hyperkalaemia in adults — triage and diagnostic approach

A result on a screen, usually in a well patient. Decide the urgency from the level and the ECG together, exclude a spurious sample, find the cause, then protect the drugs that are protecting the kidney and heart.
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AdultsLab resultK⁺ above 5.5v1.0 · Sep 2026
Core rule. K⁺ ≥6.5 mmol/L is a medical emergency at any level of wellness, and any ECG change at any potassium is an emergency — admit, do not repeat the sample first. Below that, the level and the ECG together set the urgency: 6.0–6.4 is same-day assessment, 5.5–5.9 in a well patient with no AKI can be managed in primary care. Two questions follow every raised result: is it real (haemolysis, a fist-clenched or delayed sample) and is there AKI. Never act on a critical value by booking a repeat — act, then confirm.
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On seeing the result: is this an emergency now? Arrange emergency admission — 999 or immediate discussion with the acute team
K⁺ ≥6.5 mmol/L, however well the patient seems · any ECG change at any potassium — peaked or tented T waves, flattened or absent P waves, broad QRS, bradycardia, sine-wave pattern · palpitations, syncope, chest pain or new arrhythmia · muscle weakness, flaccid paralysis or paraesthesiae · features of AKI — oliguria, new confusion, volume depletion, rapidly rising creatinine · suspected rhabdomyolysis, crush injury, tumour lysis or massive haemolysis · known dialysis patient with a missed session. Do the ECG if it does not delay transfer, stop the culprit drugs, and hand over the potassium, the eGFR and the drug list.
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Before anything else: is the result real, and how urgent? Two questions, in this order — but a critical value is acted on first and confirmed after

Could it be spurious?

Pseudohyperkalaemia — haemolysed sample, fist clenching or tourniquet, delay or cold in transit, thrombocytosis or leucocytosis, sampling above a drip. Ask the lab whether the sample was haemolysed. A clean repeat is reasonable only below 6.5, in a well patient with no AKI.

Urgency by level and ECG

≥6.5, or any ECG change: emergency admission. 6.0–6.4: ECG today and same-day assessment. 5.5–5.9: primary care if asymptomatic, well and no AKI. The ECG is part of triage, not a later test.

Is the kidney failing?

Compare creatinine and eGFR with previous values and look at the trend. Oliguria, volume depletion, sepsis, obstruction, or recent NSAID or contrast exposure make this AKI — which changes the destination regardless of the potassium.

What is the patient on?

ACE inhibitor or ARB, spironolactone or eplerenone, amiloride, sacubitril–valsartan, potassium supplements, trimethoprim, NSAIDs, heparin, ciclosporin or tacrolimus, beta-blockers, digoxin · potassium-containing salt substitutes.
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Red-flag screen: trigger → concern → destination → what to do before handover One row is enough; do not add up reassuring features
Trigger / red flagLeading concern · destinationDo now · do not delay
K⁺ 6.5 mmol/L or above, whatever the symptoms and however well the patient looks; or any ECG change at any potassium level. Risk of fatal arrhythmia — needs calcium, insulin–dextrose and monitoring
Emergency admission now		 Do not repeat the sample first and do not wait for a result the next day. 12-lead ECG if it does not delay transfer; a normal ECG does not make a K⁺ of 6.5 safe. Stop ACE inhibitors, ARBs, spironolactone, amiloride, potassium supplements, trimethoprim and NSAIDs now, and say on the handover what was stopped. Record the previous potassium and eGFR so the trend travels with the patient.
Hyperkalaemia with AKI: oliguria or anuria, rising creatinine, volume depletion, sepsis, urinary obstruction, recent contrast or an NSAID course; or known CKD stage 4–5 with a new rise. Acute kidney injury with hyperkalaemia · obstruction
Emergency admission if K⁺ ≥6.0, oliguric or unwell Same-day assessment otherwise		 Examine for a palpable bladder and assess volume status. Send or review U&E, bicarbonate, glucose, FBC and CRP the same day. Stop nephrotoxics. Hyperkalaemia with AKI is a nephrology or acute-medicine problem, not one to recheck in a week.
Rhabdomyolysis, crush injury, extensive burns, massive haemolysis or tumour lysis: severe muscle pain, dark urine, recent immobility or a long lie, recent chemotherapy or a high-grade malignancy. Massive potassium release · tumour lysis syndrome
Emergency admission now		 The potassium will keep rising, so the trend is the danger rather than the current value. Check CK, urate, phosphate, calcium and LDH via the acute route. Say "query rhabdomyolysis" or "query tumour lysis" on the handover so fluids are started early.
K⁺ 6.0–6.4 mmol/L with a normal ECG in a patient who is well, or a rise on repeat testing. Moderate hyperkalaemia — needs assessment today
ECG today and same-day clinical assessment		 ECG the same day, not "at the next appointment". Stop or hold the contributing drugs and review the whole list including over-the-counter NSAIDs and salt substitutes. Repeat U&E within 24 hours with a clean, promptly delivered sample. Dietary potassium restriction with written advice. If the repeat is still ≥6.0, or the ECG is abnormal, it becomes an admission.
Adrenal or endocrine cause suspected: hyperkalaemia with hyponatraemia, postural hypotension, fatigue, weight loss, pigmentation, hypoglycaemia; or after stopping long-term steroids. Addison's disease · adrenal crisis · hypoaldosteronism
999 if hypotensive, vomiting or acutely unwell Same-day endocrine advice and a 9 am cortisol		 The combination of a high potassium and a low sodium in an unwell patient is an adrenal crisis until excluded — it is missed because each number looks mild alone. Do not wait for a short Synacthen test before treating a crisis; send the patient in. Never stop long-term steroids abruptly.
Type 4 renal tubular acidosis or a drug interaction pattern: hyperkalaemia with a low bicarbonate and a normal anion gap; diabetes with modest CKD; recent trimethoprim, heparin, calcineurin inhibitor or high-dose NSAID. Hyporeninaemic hypoaldosteronism · drug-induced tubular defect
Same-day drug review; nephrology advice if persistent		 Check bicarbonate and glucose. Trimethoprim is a common and reversible culprit — switch the antibiotic rather than accepting the potassium. Persistent hyperkalaemia with a low bicarbonate in diabetic CKD needs nephrology advice, not repeated rechecks.
Heart-failure or CKD patient in whom the drugs are the treatment: a rise after starting or up-titrating an ACE inhibitor, ARB, sacubitril–valsartan or an MRA. Expected drug effect versus unsafe level — the decision is which drug, at what dose
Same-day review of drug and dose; specialist advice before abandoning an MRA		 A modest, stable rise after starting a renin–angiotensin blocker is expected and does not automatically mean stopping the drug — these agents reduce mortality, and blanket withdrawal causes harm. Follow the CKD/heart-failure monitoring rules, recheck within 1–2 weeks, and seek cardiology or renal advice about dose reduction or a potassium binder before stopping outright.
Unexplained renal impairment with systemic features: weight loss, bone pain, anaemia, hypercalcaemia, night sweats or lymphadenopathy behind the raised potassium. Myeloma · malignancy presenting through renal impairment
Very urgent myeloma screen — FBC, calcium, ESR/plasma viscosity, serum protein electrophoresis and urine Bence Jones protein · NICE NG12		 Hyperkalaemia is not itself an NG12 criterion, but the renal impairment behind it may be the presentation of myeloma. Send the myeloma screen as a very urgent investigation and refer urgently if abnormal (NG12). Do not stop at correcting the potassium.
Safety rule. Wellness is not reassurance: patients with K⁺ of 7 often feel normal until the arrhythmia. A normal ECG does not make a high potassium safe, and a normal potassium on a haemolysed repeat does not undo a genuine previous result. If a row applies and the safe destination is unavailable, escalate rather than recheck.
Colour is semantic: red = emergency now · amber = same-day assessment · blue = define/assess · green = primary-care management · purple = uncertain / specialist route (including 2WW). Continued on page 2: examination and tests, classification, cause classifier, routine referral, primary-care management, endpoint.
REASONING GP · Hyperkalaemia in adults — triage and diagnostic approach
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Assessment and investigation A result reviewed remotely still needs an ECG and a face-to-face assessment above 6.0

ECG — what to look for

In order of progression: tall peaked T waves → flattened or absent P waves and PR prolongation → broad QRS → sine wave and asystole. Also bradycardia and any new arrhythmia. Changes can appear at any level and their absence never excludes risk.

Clinical assessment

Volume status and BP including postural drop, pulse and rhythm, palpable bladder, muscle power and reflexes, capillary glucose. Look for the Addisonian picture — pigmentation, weight loss, postural hypotension.

Bloods

Repeat U&E with a clean unclenched sample delivered promptly, bicarbonate, glucose, calcium, magnesium, FBC and CRP; CK if muscle symptoms; 9 am cortisol if the sodium is also low. Ask the lab about haemolysis.

Do not do

Do not delay treatment to repeat a critical value. Do not use a potassium binder to keep an unsafe level tolerable without specialist input. Do not recheck at 2 weeks at ≥6.0. Do not stop a mortality-reducing drug on a single mild rise.
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Classify: three exits, not two "Repeat in a week" is only an answer for the mild, well, no-AKI group

Emergency or same-day

K⁺ ≥6.5, any ECG change, AKI, rhabdomyolysis or tumour lysis, adrenal crisis, or 6.0–6.4 needing assessment today. Output: destination, potassium and eGFR with previous values, ECG findings, and every drug stopped with the time.

Mild, manageable in primary care

K⁺ 5.5–5.9, asymptomatic, well, no AKI, normal ECG, cause identified and modifiable. Output: cause, drugs and diet changed, repeat date, and what result triggers escalation.

Unclassified or recurrent

Persistent despite drug and diet changes, a level limiting a needed ACE inhibitor or MRA, or no cause found. Output: state the uncertainty, take the §6 route, name the reviewer and timeframe.
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Cause classifier: spurious, shifted, retained, or loaded Only once the urgency is settled
Spurious (pseudohyperkalaemia)Haemolysis, fist clenching or prolonged tourniquet, delay or cold in transit, marked thrombocytosis or leucocytosis, sampling above a drip. Patient well, normal ECG, normal previous potassium. Confirm with a clean repeat — acceptable only below 6.5 with no AKI.
Reduced excretion — drugsThe commonest real cause in primary care: ACE inhibitor, ARB, sacubitril–valsartan, spironolactone or eplerenone, amiloride, trimethoprim, NSAIDs, heparin, ciclosporin or tacrolimus, potassium supplements. Often two or three together, plus a salt substitute the patient does not count as a medicine.
Reduced excretion — kidney and endocrineKidney: AKI or CKD stage 4–5, or obstruction — the question is always what changed (a new drug, dehydration, sepsis, obstruction) rather than the CKD itself. Endocrine: Addison's disease or hypoaldosteronism — hyperkalaemia with hyponatraemia, postural hypotension, fatigue, weight loss, pigmentation; type 4 RTA in diabetic CKD gives hyperkalaemia with a low bicarbonate and a normal anion gap.
Transcellular shift, load or releaseShift: metabolic acidosis, insulin deficiency or DKA, beta-blockers, digoxin toxicity, severe hyperglycaemia — a high potassium in a hyperglycaemic unwell patient is a DKA question first. Load or release: rhabdomyolysis, crush injury, burns, haemolysis, tumour lysis, massive transfusion; dietary excess or supplements where excretion is already impaired. Potassium-based salt substitutes in CKD are a frequent and invisible cause.
Do not conclude by default"Probably haemolysis" without asking the lab, or at ≥6.5. "Chronic and stable" without comparing the trend. "Diet" with a normal eGFR and no drugs — look again for adrenal or tubular causes. Never treat the number alone when hyponatraemia or a low bicarbonate sits beside it.
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Refer or seek advice routinely from this consultation Not same-day — the cases that leave by letter or advice-and-guidance; §7 is what primary care does today
Persistent hyperkalaemia despite drug and dietary measures, or recurrent episodes → nephrology (NG203) · hyperkalaemia limiting an ACE inhibitor, ARB or MRA the patient needs → renal or cardiology advice on dose reduction and on a potassium binder — patiromer or sodium zirconium cyclosilicate, which NICE supports specifically to enable continued RAAS therapy (TA623, TA599) · CKD with declining eGFR or proteinuria → nephrology · suspected Addison's or hypoaldosteronism once stable → endocrinology with the 9 am cortisol · suspected type 4 RTA in diabetic CKD → nephrology · heart failure needing an MRA where potassium is the limiting factor → the heart-failure team, not unilateral withdrawal.
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The only decisions that belong in this consultation What primary care manages today — mild hyperkalaemia in a well patient
Review every drug, including the invisible onesStop potassium supplements and potassium-containing salt substitutes (LoSalt and similar) — patients do not report these as medicines. Stop or switch trimethoprim, NSAIDs including over-the-counter ibuprofen, and heparin where possible. Review the dose of amiloride and of any MRA.
ACE inhibitors, ARBs and MRAs — think before stoppingThese reduce mortality in heart failure and slow CKD progression. For a mild rise: recheck, correct the other contributors, consider a dose reduction, and seek advice about a potassium binder to allow continuation (TA623, TA599). Withhold temporarily during illness with dehydration and give sick-day rules. Stop outright only where the level is unsafe or advised.
Dietary potassium, and treating the driverDiet: written advice with a dietitian referral where CKD is established — reduce bananas, oranges and juice, tomatoes and purée, potatoes (boil and discard the water), dried fruit, nuts, chocolate, coffee, beans and pulses; avoid salt substitutes entirely; do not rely on diet alone at ≥6.0. Driver: correct dehydration and constipation, treat infection, relieve obstruction, optimise glycaemic control where insulin deficiency or acidosis contributes; where AKI is resolving, recheck alongside the creatinine.
Recheck and the escalation rule — write it downRepeat U&E within 3–5 days for a mild rise (sooner if a drug was changed), with a clean unclenched sample delivered promptly. Tell the patient and the record what result triggers what: ≥6.5 or any ECG change → emergency admission; 6.0–6.4 → same-day assessment. Name who is checking the result.
What not to doDo not repeat a K⁺ of ≥6.5 instead of admitting. Do not start a potassium binder without specialist advice. Do not give calcium resonium as a community substitute for admission. Do not stop long-term steroids abruptly. Do not file a raised potassium as "borderline" without a plan and a named reviewer.
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Endpoint and documentation Finish with one of four conclusions

1 · Emergency

Admission arranged; potassium and eGFR with previous values and dates, ECG findings, volume status, every drug stopped with the time, suspected cause on the handover.

2 · Same-day

ECG done and assessment arranged today; the question being answered (AKI, drug effect, adrenal), drugs held, repeat U&E within 24 hours, who was spoken to.

3 · Mild, managed

Level, cause and eGFR recorded; drugs and diet changed; repeat date booked and escalation thresholds written in the record and told to the patient; named reviewer.

4 · Unclassified or recurrent

Uncertainty stated; §6 referral or advice-and-guidance sent, with date; interim drug plan and sick-day rules; review owner and timeframe.
Why primary-care management is safe today, in one line: K⁺ is 5.5–5.9 · asymptomatic and clinically well · no AKI — creatinine and eGFR compared with previous values · ECG normal where indicated · a modifiable cause identified and acted on · sodium, bicarbonate and glucose reviewed alongside · repeat booked within 3–5 days with a named reviewer and written escalation thresholds. Safety-net wording: contact us or 111 the same day if you develop palpitations, feel faint or black out, notice new muscle weakness or numbness, cannot keep fluids down, or pass much less urine than usual; and come for the repeat blood test even if you feel well — a high potassium usually causes no symptoms until it affects the heart. Remote and result-handling limitation. A potassium of 6.0 or above cannot be managed on the telephone: it needs an ECG and a face-to-face assessment the same day. Convert to face-to-face or emergency assessment where an ECG cannot be obtained today, the patient cannot attend for a repeat, there is vomiting, diarrhoea or reduced urine output, or the result arrives out of hours with no one able to act — a critical potassium must never sit in an inbox overnight.
Clinical decision support only; follow local acute-transfer, renal and prescribing policies and check doses against the current BNF. Source hierarchy: NICE guidelines and CKS first, then BNF/MHRA for doses and safety, then national specialty guidance. Sources: NICE NG203 Chronic kidney disease · NG148 Acute kidney injury · NG106 Chronic heart failure · NG12 Suspected cancer (May 2025) · TA623 patiromer · TA599 sodium zirconium cyclosilicate · NICE CKS Hyperkalaemia, Chronic kidney disease, Addison's disease · UK Kidney Association guideline on acute hyperkalaemia in adults · Resuscitation Council UK · BNF · MHRA. Review after any guidance or medicines-safety update, otherwise every 6 months. © Reasoning GP · gpreasoning.uk